Metformin in the ileum
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA828119 | ENA |
REPOSITORIES: ENA
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Project description:C57BL/6J male mice were treated with or without metformin
2022-04-20 | GSE201039 | GEO
Project description:Metformin is the therapy of choice for treating type 2 diabetes and is currently repurposed for a wide range of diseases including aging. Recent evidence implicates the gut microbiota as a site of metformin action. Combining two tractable genetic models, the bacterium E. coli and the nematode C. elegans, we performed C. elegans RNAseq to investigate the role of the metformin sensitive OP50 and metformin resistant OP50-MR E. coli microbiota in the drug effects on the host. Our data suggest an evolutionarily conserved bacterial mediation of metformin effects on host lipid metabolism and lifespan.
2019-07-13 | E-MTAB-7272 | biostudies-arrayexpress
Project description:Research findings of the past decade have highlighted the gut as the main site of action of the oral antihyperglycemic agent metformin despite its pharmacological role in the liver. Extensive evidence supports metformin’s modulatory effect on the composition and function of gut microbiota, nevertheless, the underlying mechanisms of the host responses remain elusive. Our study aimed to evaluate metformin-induced alterations in the intestinal transcriptome profiles at different metabolic states. The high-fat diet-induced type 2 diabetes mouse model of both sexes was developed in a randomized block experiment and bulk RNA-Seq of the ileum tissue was the method of choice for comparative transcriptional profiling after metformin intervention for ten weeks. We found a prominent transcriptional effect of the diet itself with comparatively fewer genes responding to metformin intervention. The overrepresentation of immune-related genes was observed, including pronounced metformin-induced upregulation of immunoglobulin heavy-chain variable regioncoding Ighv1-7 gene in both high-fat diet and control diet-fed animals, supporting the contribution of intestinal immunoglobulin responses. Finally, we provide evidence of the downregulation NF-kappa B signaling pathway in the small intestine of both hyperglycemic and normoglycemic animals after metformin treatment. Moreover, our data pinpoint the gut microbiota as a crucial component in the metformin-mediated downregulation of NF-kappaB signaling evidenced by a positive correlation between the Rel and Rela gene expression levels and abundances of Parabacteroides distasonis, Bacteroides spp., and Lactobacillus spp. in the gut microbiota of the same animals.
2023-08-12 | GSE240206 | GEO
Project description:Metformin on human macrophages Human blood derived macrophages were treated with 10micromolar Metformin (Sigma-Aldrich) for 4h
2020-06-27 | GSE153318 | GEO
Project description:Metformin has been commonly used for decades to treat type 2 diabetes. Recent data indicates that mice treated with metformin live longer and healthier lives. Here, we show that chronic metformin exposure in mice and diabetics taking metformin have higher levels of the microRNA processing protein, Dicer. Examination of how metformin affects Dicer expression revealed that metformin alters binding of the AUF1 RNA-binding protein to DICER1 mRNA, which leads to stabilization of DICER1 mRNA. We found differential changes in microRNA expression in mice treated with metformin or caloric restriction, a proven life extending intervention. Several of these microRNAs are important for regulating cellular senescence and lifespan in model organisms. Consistent with this observation, treatment with metformin decreased cellular senescence in a Dicer-dependent manner. These data lead us to hypothesize that changes in Dicer levels may be important for organismal aging and that interventions that upregulate Dicer expression (e.g., metformin) may offer new therapeutic approaches to combat or prevent age-related diseases. Key words: diabetes mellitus, metformin, senescence, miRNA, RNA-binding proteins
2017-02-14 | GSE73393 | GEO
Project description:Reduced cancer incidence has been reported among type II diabetics treated with metformin. Metformin exhibits anti-proliferative and anti-neoplastic effects associated with inhibition of mTORC1, but the mechanisms are poorly understood. We provide the first genome-wide analysis of translational targets of canonical mTOR inhibitors (rapamycin and PP242) and metformin, revealing that metformin controls gene expression at the level of mRNA translation to an extent comparable to that of canonical mTOR inhibitors. Importantly, metformin's anti-proliferative activity can be explained by selective translational suppression of mRNAs encoding cell cycle regulators via the mTORC1/4E-BP pathway. Thus, metformin selectively inhibits mRNA translation of encoded proteins that promote neoplastic proliferation, motivating further studies of this compound and related biguanides in cancer prevention and treatment. MCF7 cells were treated with rapamycin, metformin or PP242 at concentrations that inhibited proliferation to 50% of control. Both cytoplasmic and polysome-associated mRNA was extracted from treatments and a vehicle treated control and probed with microarrays.
2012-05-20 | E-GEOD-36847 | biostudies-arrayexpress
Project description:This study is a comparative proteomics study of FACS sorted Muc2 expressing and non expressing cells in mouse ileum and colon.
2021-04-19 | PXD011527 | Pride
Project description:Optimal treatment for nonalcoholic steatohepatitis (NASH) has not yet been established, particularly for individuals without diabetes. We examined the effects of metformin, commonly used to treat patients with type 2 diabetes, on liver pathology in a non-diabetic NASH mouse model. Eight-week-old C57BL/6 mice were fed a methionine- and choline-deficient (MCD) + high fat (HF) diet with or without 0.1% metformin for 8 weeks.
2012-02-21 | E-GEOD-35961 | biostudies-arrayexpress
Project description:Objective: To investigate the effects of metformin on intestinal carbohydrate metabolism in vivo.
Method: Male mice preconditioned with a high-fat, high-sucrose diet were treated orally with metformin or a control solution for two weeks. Fructose metabolism, glucose production from fructose, and production of other fructose-derived metabolites were assessed using stably labeled fructose as a tracer.
Results: Metformin treatment decreased intestinal glucose levels and reduced incorporation of fructose-derived metabolites into glucose. This was associated with decreased intestinal fructose metabolism as indicated by decreased enterocyte F1P levels and diminished labeling of fructose-derived metabolites. Metformin also reduced fructose delivery to the liver. Proteomic analysis revealed that metformin coordinately down-regulated proteins involved carbohydrate metabolism including those involved in fructolysis and glucose production within intestinal tissue.
Conclusion: Metformin reduces intestinal fructose metabolism, and this is associated with broad-based changes in intestinal enzyme and protein levels involved in sugar metabolism indicating that metformin's effects on sugar metabolism are pleiotropic.
2024-04-27 | PXD041833 | JPOST Repository